糖尿病高血压与原发性高血压胰岛素抵抗及高胰岛素血症的对比研究

目的 探讨糖尿病高血压与原发性高血压患者胰岛素抵抗与高胰岛素血症的关系。方法 测定４２例原发性高血压（ＥＨ）、２９例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）、１６例ＮＩＤＤＭ合并高血压（ＤＨＰ）患者的胰岛素敏感性指数（ＩＳＩ）和血浆胰岛素（ＩＮＳ）水平,结果 ＤＨＰ组与ＮＩＤＤＭ组的胰岛素抵抗相似,但前者血浆ＩＮＳ水平明显高于后者,虽然ＥＨ组的ＩＳＩ显著高于ＮＩＤＤ几ＤＨＰ组,但同时其ＩＮＳ分泌量也明显     

糖原合成酶与NIDDM

非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者存在糖原合成酶（ＧＳ）的合成和活化障碍，这是导致胰岛素抵抗（ＩＲ）的主要原因。动物实验和糖尿病一级亲属的前瞻性研究表明，ＧＳ基因缺陷可能是ＮＩＤ－ＤＭ的遗传缺陷。近年来分子遗传学研究发现，部分种族及部分人群ＮＩＤＤＭ的发生与ＧＳ基因变异密切相关     

糖原合成酶与NIDDM

非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者存在糖原合成酶（ＧＳ）的合成和活化障碍，这是导致胰岛素抵抗（ＩＲ）的主要原因。动物实验和糖尿病一级亲属的前瞻性研究表明，ＧＳ基因缺陷可能是ＮＩＤＤＭ的遗传缺陷。近年来分子遗传学研究发现，部分种族及部分人群ＮＩＤＤＭ的发生与ＧＳ基因变异密切相关。     

糖尿病基因治疗的研究

糖尿病基因治疗的研究肖新华，王糖尿病主要分两大类：胰岛素依赖型糖尿病（ＩＤ－ＤＭ）和非胰岛素依赖型糖尿病（ＮＩＤＤＭ），其共同特点表现在维持正常血糖所需的精确的、时限性的胰岛素释放的缺陷。两者胰岛素释放缺陷的发病基础完全不同，ＩＤＤＭ涉及自身免疫介导...     

非胰岛素依赖型糖尿病并发冠心病患者血脂、脂蛋白及载脂蛋白A_1、B测定的临床意义

非胰岛素依赖型糖尿病并发冠心病患者血脂、脂蛋白及载脂蛋白Ａ_１、Ｂ测定的临床意义曹承清（长沙市第一医院）本文采用酶法及透射比浊法对６２例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者（其中单纯ＮＩＤＤＭ２８例，ＮＩＤＤＭ合并冠心病３４例）进行了清晨空腹血清甘?..     

非胰岛素依赖型糖尿病肾病肾组织中EGF、EGF－R和IGF－1R的检测及其意义

应用免疫组织化学定量分析的方法，对１２例胰岛素非依赖型糖尿病（ＮＩＤＤＭ）肾病患者肾活检组织中胰岛素样生长因子－１（ＩＧＦ－１）受体、表皮生长因子（ＥＧＦ）和表皮生长因子受体（ＥＧＦ－Ｒ）进行了观察，并结合患者的病程、糖尿病肾病分期和肾功能进行了比较。ＮＩＤＤＭ肾病患者肾小管上ＥＧＦ和ＥＧＦ－Ｒ的量明显高于正常人，部分患者肾小球ＥＧＦ也呈阳性反应。正常人和ＮＩＤＤＭ肾病患者肾小管上ＩＧＦ－１受体的量则无明显差异。提示肾小管上ＥＧＦ和ＥＧＦ－Ｒ含量增加可能参与ＮＩＤＤＭ肾病的发病过程，而肾小球内ＥＧＦ的出现与系膜细胞和系膜基质增生有关。     

少儿非胰岛素依赖型糖尿病研究进展

以往学者们认为,少儿糖尿病（ＤＭ）是由于遗传因素造成胰岛β细胞变性,使胰岛素产生和释放降低所致,属胰岛素依赖型糖尿病（ＩＤＤＭ）;成人ＤＭ则是由于血中胰岛素拮抗物增多或胰岛素失活而使体内胰岛素增多所致,属非胰岛素依赖型糖尿病（ＮＩＤＤＭ）。但近年来的研究发现,ＮＩＤＤＭ在少儿ＤＭ中并不少见。１９９６年１２月在美国举行的首届国际少儿ＤＭ学术会议上,正式确定了少儿ＮＩＤＤＭ的概念〔１〕。１　少儿ＮＩＤＤＭ的发病情况少儿ＮＩＤＤＭ主要发生于有色人种。１９８８～１９９５年美国阿肯色州共发现少儿ＮＩＤＤＭ…     

糖尿病合并心律失常患者的心钠素水平测定及临床意义

作者用放射免疫分析对２４例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）合并心律失常患者进行血浆心钠素（ＡＮＦ）、空腹血胰岛素及餐后２小时血胰岛素水平测定，结果表明ＮＩＤＤＭ合并心律失常患者血ＡＮＦ水平、空腹及餐后胰岛素均高于无心律失常组，且均呈高度显著性差异（Ｐ〈０．０１）。提示糖尿病合并心律失常时血ＡＮＦ有明显升高，高胰岛素血症与糖尿病心脏病变有关。     

血、尿β_2微球蛋白测定在早期糖尿病肾病诊断中的意义

血、尿β２微球蛋白测定在早期糖尿病肾病诊断中的意义广东省汕头大学医学院第二附属医院内分泌科（５１５０３１）杨毅华陈惠明糖尿病肾病（ＤＮ）是糖尿病的严重并发症之一。不论是胰岛素依赖型糖尿病（ＩＤＤＭ）或非胰岛素依赖型糖尿病（ＮＩＤＤＭ），若血糖控制不良...     

Ⅱ型糖尿病合并高血压患者高胰岛素血症和舒血管前列腺…

对２３例非胰岛素依赖型糖尿病（ＮＩＤＤＭ）患者，１８例ＮＩＤＤＭ合并高血压的和１８例正常人在糖耐量试验期间血胰岛素、６－酮－前列腺素Ｆ１α（６－ｋｅｔｏ－ＰＧＥ１α）和前列腺素Ｅ２（ＰＧＥ２）水平进行了测定。提示ＮＩＤＤＭ合并高血压可能与高胰岛素血症抑制舒血管前列腺素合成有关。     

Ambient plasma free fatty acid concentrations in noninsulin-dependent diabetes mellitus: evidence for insulin resistance

Plasma glucose, insulin, and FFA concentrations were determined in 15 normal subjects and 15 patients with noninsulin-dependent diabetes mellitus (NIDDM) from 0800 to 1600 h. Breakfast and lunch were consumed at 0800 and 1200 h, respectively, and plasma concentrations were measured at hourly intervals from 0800-1600 h. Plasma glucose concentrations between 0800 and 1600 h were significantly elevated in patients with NIDDM, and the higher the fasting glucose level, the greater the postprandial hyperglycemia. Hyperglycemia in patients with NIDDM was associated with plasma insulin levels that were significantly higher (P less than 0.001) than those in normal subjects, and substantial hyperinsulinemia occurred between 0800 and 1600 h in patients with mild NIDDM (fasting plasma glucose concentrations, less than 140 mg/dl). Both fasting and postprandial FFA levels were also increased in patients with NIDDM (P less than 0.001), and the greater the plasma glucose response, the higher the FFA response (r = 0.70; P less than 0.001). However, there was no significant correlation between plasma insulin and FFA concentrations. More specifically, hyperinsulinemic patients with mild diabetes (fasting plasma glucose, less than 140 mg/dl) maintained normal ambient FFA levels, while FFA concentrations were significantly elevated in patients with severe NIDDM (fasting plasma glucose, greater than 250 mg/dl), with insulin concentrations comparable to those in normal subjects. These results demonstrate that patients with NIDDM are not capable of maintaining normal plasma FFA concentrations. This defect in FFA metabolism is proportionate to the magnitude of hyperglycemia and occurs despite the presence of elevated levels of plasma insulin. These results are consistent with the view that insulin resistance in NIDDM also involves the ability of insulin to regulate FFA metabolism.     

2型糖尿病患者血中甲状旁腺高血压因子的研究

目的 探讨２型糖尿病患者血中是否存有甲状旁腺高血压因子（ＰＨＦ）活性异常及其与胰岛素抵抗的关系。方法 采用生物活性测定方法，检测３２例２型糖尿病患者和３３名正常人血浆中ＰＨＦ活性。结果 ２型糖尿病患者血中平均ＰＨＦ活性显著高于对照组，但未能确定与胰岛素抵抗之间的关系。结论 部分２型糖尿病患者血中存有异常高水平的ＰＨＦ，其作用机制有待进一步研究。     

继发性磺脲类失效糖尿病患者胰岛素释放及外周胰岛素敏感度的研究

本文应用７５ｇ葡萄糖耐量试验对１８例继发性磺脲类药物治疗失效ＮＩＤＤＭ患者的胰岛素释放及外周胰岛素敏感度进行了测算，结果发现，继发性磺脲类失效ＮＩＤＤＭ患者的胰岛素释放和外周胰岛素敏感度均显著低于磺脲类药物治疗有效的ＮＩＤＤＭ患者及正常对照。提示继发性磺脲类失效ＮＩＤＤＭ患者存在明显的胰岛素分泌功能损害和外周胰岛素抵抗。     

Growth hormone-binding protein related immunoreactivity is regulated by the degree of insulinopenia in diabetes mellitus

OBJECTIVE Derangements in the GH/IGF axis are common in patients with diabetes mellitus. In insulin-dependent diabetes mellitus (IDDM), these disturbances seem to be due to a partial defect in GH action on its own receptor or via a post-receptor defect. In non-insulin-dependent diabetes mellitus (NIDDM), data are limited, and the regulation of the GH receptor (GHR) remains unclear. However, animal studies with diabetic rats demonstrated that the GHR density may be influenced by insulin disposal at the hepatocyte. With respect to this hypothesis we studied the relation between peripheral insulin status and the serum GH-binding protein (GHBP), which reflects indirectly the GHR density in the tissues. Patients with IDDM were compared to a NIDDM group as well as to a group of healthy subjects. DESIGN AND PATIENTS Basal blood samples for the determination of serum GHBP, GH, and IGF-I were obtained from patients with IDDM (n = 27), subjects with NIDDM (n = 112) and healthy controls (n = 42). Insulin, proinsulin, C-peptide and IGF-binding protein 1 (IGFBP-1) serum levels were used to estimate the insulin status in diabetic patients. RESULTS GHBP serum levels were significantly lower in patients with IDDM than in either NIDDM or controls (P < 0.001). Conversely, the IGF-I levels were reduced in both groups of diabetics. A subgroup of hypoinsulinaemic NIDDM patients showed significantly decreased GHBP concentrations (P < 0.05) compared to the NIDDM subgroup with hyperinsulinaemia. Furthermore, GHBP levels were significantly decreased in insulin-treated patients with NIDDM compared to either non-insulin-requiring subjects or normal controls (P < 0.05). A significant direct relation was found between levels of GHBP and total insulin dose (P < 0.01) in patients with IDDM. In the NIDDM group, GHBP was correlated with proinsulin (P < 0.001), C-peptide (P < 0.01), insulin (P < 0.05) and inversely with IGFBP-1 (P < 0.001). Multiple linear regression analysis indicated a significant contribution of proinsulin and IGFBP-1 to the variation of GHBP. CONCLUSIONS Decreased GHBP levels in IDDM as well as in NIDDM correlate with insulinopenia. Since the degree of insulinopenia depends on the capability of the β-cells to secrete proinsulin, C-peptide and insulin, we hypothesize that these hormones at least partially influence the serum level of GHBP. Low GHBP levels may reflect a reduced GH receptor density and a concomitant GH insensitivity, which leads to an impaired IGF generation in insulin-deficient patients.     

Hepatic extraction of insulin in non-insulin dependent diabetes. Comparative study of obese and non-obese patients

Changes in the secretion and metabolism of insulin were measured by estimating serum C-peptide and insulin and their ratio during oral GTT in 30 non obese and 12 obese NIDDM patients. The mean IRI and CP responses were low in both groups of patients, compared to weight-matched controls. The reduction in CP was more marked than the reduction in IRI. The molar ratio of insulin and CP was found to be elevated in the patients, probably indicating reduced hepatic and peripheral extraction of insulin. It was noted that the elevated IRI/CP ratio was a 1) a common feature in NIDDM, irrespective of the body weight, 2) it is present even under basal conditions when the insulin levels are the lowest, 3) it appears to be independent of the concentration of insulin reaching the liver, and 4) obese patients appear to have an exaggerated defect compared to their non obese counterparts.     

C-peptide secretion in calcific tropical pancreatic diabetes

Serum C-peptide levels were measured during a glucagon stimulation test in ten normal nonobese controls and 54 diabetic patients with recent onset of diabetes under 30 years of age. Diabetic patients were comprised of 13 CTPD, 23 IDDM, and 18 NIDDM. As similar to IDDM patients, serum C-peptide concentrations did not rise significantly (P greater than 0.05) in response to glucagon administration in CTPD-patients. Mean baseline and peak serum C-peptide concentrations in CTPD-patients were significantly lower (P less than 0.001) than the values in normal controls and NIDDM patients, but were significantly higher (P less than 0.05) than those in IDDM patients. We conclude that CTPD patients have partial C-peptide reserve, which may protect against ketosis and contribute to ketosis resistance in CTPD. Our results also suggest that CTPD patients require insulin treatment. Neither baseline nor peak C-peptide levels after glucagon could discriminate CTPD from IDDM and CTPD from NIDDM.     

Resistance to insulin suppression of plasma free fatty acid concentrations and insulin stimulation of glucose uptake in noninsulin-dependent diabetes mellitus

The ability of insulin to stimulate tissue glucose uptake and lower plasma FFA concentrations was quantified in 12 individuals with normal glucose tolerance and 12 patients with noninsulin-dependent diabetes mellitus (NIDDM), further subdivided into obese and nonobese subjects. Measurements were made during 5-h glucose clamp studies, carried out at plasma insulin concentrations of about 10 microU/ml (0-150 min) and about 60 microU/ml (150-300 min). Differences between the patient groups were compared by two-way analysis of variance. The ability of insulin to either suppress plasma FFA concentrations or stimulate glucose uptake was significantly reduced (P less than 0.001) in patients with NIDDM, and this was true of both the obese and nonobese groups. The defect in the ability of insulin to suppress plasma FFA concentrations in patients with NIDDM was more apparent at the lower insulin concentration, whereas resistance to insulin-stimulated glucose uptake in NIDDM was more dramatic at the high insulin concentration. Finally, a significant correlation (r = -0.67; P less than 0.001) between insulin-stimulated glucose uptake and plasma FFA concentration was found in the entire group. These data emphasize the fact that patients with NIDDM are resistant to multiple actions of insulin, and that the magnitudes of the defect in insulin suppression of plasma FFA levels and stimulation of tissue glucose uptake are roughly comparable.     

Effect of differences in glucose tolerance on insulin's ability to regulate carbohydrate and free fatty acid metabolism in obese individuals

The effect of variations in glucose tolerance on insulin's ability to regulate glucose uptake and plasma glucose and FFA concentrations was assessed in 22 obese individuals [8 with normal glucose tolerance, 7 with impaired glucose tolerance (IGT), and 7 with noninsulin-dependent diabetes mellitus (NIDDM)]. Patients with IGT had ambient insulin levels that were higher than normal, associated with elevated postprandial glucose levels and a marked reduction in insulin-stimulated glucose uptake. On the other hand, plasma FFA levels were relatively normal in IGT, possibly because of the hyperinsulinemia. Patients with NIDDM were also hyperinsulinemic, with insulin levels throughout the day that were approximately twice normal. Hyperinsulinemia in patients with NIDDM was associated with a significant decline in insulin-stimulated glucose uptake as well as with significant increases in both ambient plasma glucose and FFA concentrations. Thus, and in contrast to patients with IGT, plasma FFA metabolism in NIDDM was grossly abnormal, despite the concomitant hyperinsulinemia. These data indicate that insulin resistance in obese individuals varies as a function of degree of glucose tolerance, and insulin resistance in patients with NIDDM involves defects in the regulation of both plasma glucose and FFA metabolism.     

The intracellular mechanism of insulin resistance in pancreatic cancer patients

The diabetes that frequently occurs in pancreatic cancer patients is characterized by profound peripheral insulin resistance. The intracellular mechanism of this insulin resistance was investigated in skeletal muscle biopsies from pancreatic cancer patients with or without diabetes and control subjects. Insulin receptor (IR) binding, tyrosine kinase activity, IR messenger RNA (mRNA), IR substrate-1 content, GLUT-4, and GLUT-4 mRNA content were all normal in pancreatic cancer patients. In contrast, multiple defects in glycogen synthesis were found in pancreatic cancer patients, especially in those with diabetes. Glycogen synthase I activity, total activity, and mRNA levels were significantly decreased in pancreatic cancer patients compared with controls. The fractional velocity of glycogen synthase was decreased only in the diabetic pancreatic cancer group. Glycogen phosphorylase a and b activities were increased in diabetic pancreatic cancer patients, but glycogen phosphorylase mRNA levels were not significantly different. The insulin resistance associated with pancreatic cancer is associated with a post-IR defect, which impairs skeletal muscle glycogen synthesis and glycogen storage.     

冠状动脉粥样硬化性心脏病中胰岛素的抵抗性

为探索冠心病中有无胰岛素抵抗性/高胰岛素血症及其在冠状动脉粥样硬化发生发展过程中的作用,本文检测了32例非肥胖、口服葡萄糖耐量试验正常的单纯冠心病患者在服糖前后的血浆胰岛素、甘油三脂、总胆固醇浓度。结果表明,冠心病组病人存在餐后高胰岛素血症,血脂升高,这提示高胰岛素血症/胰岛素抵抗性可能是非糖尿病者发生冠心病的一个危险因素。